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EMERGENT
Endocrine
ICU
Diabetic Ketoacidosis (DKA)
Life-threatening metabolic emergency requiring early recognition, aggressive IV fluids, insulin infusion, and electrolyte replacement -with vigilant monitoring for complications.
RoundsRx Licensed Content - Unauthorized Use Prohibited🔍 Overview
Definition
DKA is characterized by the triad of hyperglycemia (usually BG > 250 mg/dL), anion-gap metabolic acidosis (pH < 7.3, bicarb < 18), and ketonemia/ketonuria. It results from absolute or relative insulin deficiency combined with excess counterregulatory hormones.
Why It Matters
⚠ Mortality up to 5% in adultsHigher in elderly, delayed recognition, or severe comorbidities. Cerebral edema is the leading cause of death in children.
Who Gets It
- Type 1 DM (can be the presenting illness in ~25%)
- Type 2 DM under physiologic stress
- SGLT2-inhibitor users (euglycemic DKA -BG may be < 200!)
- Precipitants: infection (30–40% -most common), insulin omission/non-compliance (20–25%), new diagnosis T1DM, MI/ACS, pancreatitis, cocaine, alcohol
Mnemonic -5 I's of DKA Precipitants:
Infection (30–40%, #1 cause -UTI, pneumonia, skin) · Insulin (missed or inadequate doses) · Infarction (MI, stroke, mesenteric ischemia) · Intoxication (cocaine, alcohol, drugs) · Inflammation (pancreatitis, surgery, trauma)
Infection (30–40%, #1 cause -UTI, pneumonia, skin) · Insulin (missed or inadequate doses) · Infarction (MI, stroke, mesenteric ischemia) · Intoxication (cocaine, alcohol, drugs) · Inflammation (pancreatitis, surgery, trauma)
Pathophysiology
Insulin deficiency → unrestrained lipolysis → free fatty acids → hepatic ketogenesis (acetoacetate, β-hydroxybutyrate) → high anion gap metabolic acidosis. Hyperglycemia → osmotic diuresis → profound volume depletion and electrolyte losses. Total body K⁺ is depleted even when serum K⁺ appears normal or high (due to transcellular shift from acidosis).
Presentation
Symptoms
- Polyuria, polydipsia, nausea, vomiting, abdominal pain
- Weakness, fatigue, altered mental status (in severe cases)
- Timeline: hours to days (faster than HHS)
Exam
- Kussmaul respirations (deep, rapid -compensating for acidosis)
- Fruity/acetone breath
- Signs of dehydration: dry mucosa, tachycardia, hypotension, poor skin turgor
Red Flags
- Altered mental status → think cerebral edema, severe osmolarity
- Potassium < 3.5 → do NOT start insulin until repleted
- Euglycemic DKA (SGLT2i) -don't miss it
- pH < 7.0 or bicarb < 10 → severe DKA, ICU threshold
Differential Diagnosis
- HHS -BG often > 600, severe hypertonicity, no/minimal ketones, pH usually > 7.3
- Alcoholic ketoacidosis -low or normal glucose, ketones present, history of binge drinking + poor PO
- Starvation ketosis -mild, pH > 7.3, bicarb usually > 18
- Other high AG acidosis -lactic acidosis, toxic ingestions (methanol, ethylene glycol, salicylates)
🧪 Workup & Diagnosis
Initial Workup
DO ALL OF THIS IMMEDIATELYThese tests diagnose DKA, guide fluid/insulin dosing, and identify precipitant -results change management NOW.
Labs (STAT)
- BMP -BG, creatinine, K⁺, bicarbonate
- VBG or ABG -pH, pCO₂, calculated bicarb
- Anion gap = Na – (Cl + HCO₃) → normal 8–12; in DKA typically > 20
- Beta-hydroxybutyrate (BHB), serum -≥ 3.0 mmol/L is diagnostic for DKA per ADA/EASD 2024. Preferred over urine ketones for both diagnosis AND monitoring resolution.
- Urine ketones (only if serum BHB unavailable; moderate-to-large dipstick ketones is the fallback diagnostic threshold)
- Phosphate, magnesium -often depleted
- CBC, blood cultures -rule out infectious precipitant
- Lipase -DKA can elevate lipase without true pancreatitis
- HbA1c -assess chronic control
- Urinalysis + urine culture
- Pregnancy test (women of childbearing age)
Imaging / ECG
- ECG -assess for hyperkalemia changes (peaked T waves, wide QRS) or ischemia as precipitant
- CXR -rule out pneumonia as precipitant
- CT head only if focal neuro deficits or concern for cerebral edema
Diagnostic Criteria for DKA UPDATED 2024
🔄 What changed in 2024 (ADA/EASD Consensus): Diagnosis now requires all three of the triad below, with BHB ≥ 3.0 mmol/L as the preferred ketone marker. Severity grading was simplified to pH and bicarb only, anion gap and mental status were removed (AG is confounded by hyperchloremic acidosis from NS; mental status is now used for ICU triage, not severity grading). Bicarb thresholds also shifted slightly.
Diagnostic Triad (all 3 required)
- Hyperglycemia: glucose ≥ 200 mg/dL (or known diabetes; not required in euglycemic DKA on SGLT2i)
- Ketosis: BHB ≥ 3.0 mmol/L (preferred) OR moderate-to-large urine ketones
- Acidosis: venous pH < 7.3 OR serum bicarbonate < 18 mEq/L
Severity Grading (ADA/EASD 2024)
| Parameter | Mild | Moderate | Severe | vs prior guideline |
|---|---|---|---|---|
| Venous pH | 7.25–7.30 | 7.00–7.24 | < 7.00 | UNCHANGED |
| Bicarb (mEq/L) | 15–18 | 10–<15 | < 10 | CHANGED mild now 15–18 (was 15–18, but resolution threshold raised) |
| Anion gap and mental status were removed from severity grading in 2024. AG is still elevated in DKA but is confounded by hyperchloremic acidosis after NS resuscitation. Altered mental status remains an independent ICU-triage criterion. | ||||
ADA/EASD Consensus, 2024
🚨 Management
Treatment: Step by Step
BEFORE STARTING INSULINEnsure K⁺ ≥ 3.5 mEq/L. Starting insulin with hypokalemia causes fatal cardiac arrhythmia.
First 5 Minutes
Assess & Stabilize
ABCs. IV access × 2. Foley if altered or unable to void. Cardiac monitor. POC glucose. Draw all STAT labs. Call senior if severe (pH < 7.1, AMS, K⁺ < 3.5).
ABCs. IV access × 2. Foley if altered or unable to void. Cardiac monitor. POC glucose. Draw all STAT labs. Call senior if severe (pH < 7.1, AMS, K⁺ < 3.5).
First 15–30 Minutes
IV Fluids -Bolus Only If Hemodynamically Unstable
• Unstable / severely volume-depleted: 1-1.5 L isotonic crystalloid bolus over 1 hour (NS OR balanced).
• Stable: skip the bolus -start 250-500 mL/hr maintenance from the outset.
The reflex "2 L for everyone" is out; over-resuscitation is the more common modern error ADA DKA Consensus, 2024
After the first hour, choose by corrected Na⁺ (calculator):
• Corrected Na ≤ 135 → continue 0.9% NS at 250-500 mL/hr
• Corrected Na > 135 → switch to 0.45% NaCl at 250-500 mL/hr
• If using LR: just continue LR throughout and skip the half-NS switch (LR's Na 130 already provides some free water; only switch to 0.45% NaCl if corrected Na > 150).
Goal: replace 3-6 L deficit over 24-48 h (gentler is fine; over-aggressive correction risks cerebral edema, especially in pediatrics -PECARN, 2018).
• Unstable / severely volume-depleted: 1-1.5 L isotonic crystalloid bolus over 1 hour (NS OR balanced).
• Stable: skip the bolus -start 250-500 mL/hr maintenance from the outset.
The reflex "2 L for everyone" is out; over-resuscitation is the more common modern error ADA DKA Consensus, 2024
After the first hour, choose by corrected Na⁺ (calculator):
• Corrected Na ≤ 135 → continue 0.9% NS at 250-500 mL/hr
• Corrected Na > 135 → switch to 0.45% NaCl at 250-500 mL/hr
• If using LR: just continue LR throughout and skip the half-NS switch (LR's Na 130 already provides some free water; only switch to 0.45% NaCl if corrected Na > 150).
Goal: replace 3-6 L deficit over 24-48 h (gentler is fine; over-aggressive correction risks cerebral edema, especially in pediatrics -PECARN, 2018).
🔄 Updated Practice: Old teaching was NS (normal saline) for DKA fluid resuscitation. Newer evidence (SMART, 2018) suggests balanced crystalloids (LR) may be preferred -NS causes hyperchloremic metabolic acidosis, which can worsen and confuse the clinical picture. The 4 mEq/L of potassium in LR is NOT a contraindication in hyperkalemic DKA -it's below physiologic plasma K⁺, and NS paradoxically worsens hyperkalemia via hyperchloremic acidosis (shifts K⁺ out of cells). Balanced crystalloids are safe in DKA despite that potassium content, and avoid the hyperchloremic acidosis that saline adds on top of the ketoacidosis.
First Hour
Potassium Replacement
K⁺ < 3.5 → replace aggressively (20–40 mEq/hr IV), do NOT start insulin yet
K⁺ 3.5–5.0 → add 20–30 mEq K⁺ per liter of IVF, start insulin
K⁺ > 5.0 → start insulin, hold K⁺ replacement, recheck in 2 hours
Insulin Infusion
Regular insulin drip at 0.1 units/kg/hr fixed rate, no bolus required (per ADA/EASD Consensus, 2024). A 0.1 units/kg IV bolus is reserved for a delay in setting up the infusion. Target: BG drop of 50–75 mg/dL/hr.
K⁺ < 3.5 → replace aggressively (20–40 mEq/hr IV), do NOT start insulin yet
K⁺ 3.5–5.0 → add 20–30 mEq K⁺ per liter of IVF, start insulin
K⁺ > 5.0 → start insulin, hold K⁺ replacement, recheck in 2 hours
Insulin Infusion
Regular insulin drip at 0.1 units/kg/hr fixed rate, no bolus required (per ADA/EASD Consensus, 2024). A 0.1 units/kg IV bolus is reserved for a delay in setting up the infusion. Target: BG drop of 50–75 mg/dL/hr.
🔄 Updated Practice: The old DKA protocol included an insulin IV bolus before starting the drip. Current guidance recommends NO routine bolus -start a fixed-rate continuous infusion at 0.1 units/kg/hr directly (a bolus is reserved for a delay in setting up the infusion). The bolus increased hypoglycemia risk without improving outcomes. Also: subcutaneous insulin protocols (insulin lispro/aspart q1-2h) are acceptable for mild-moderate DKA -IV is not always necessary.
When BG Hits 200–250 mg/dL
Switch to Dextrose-Containing Fluids
Add D5 to IV fluids (D5-0.45%NS) -reduce insulin drip to 0.05 units/kg/hr. Continue until anion gap closes, NOT just until BG normalizes. This is the most common resident mistake.
Add D5 to IV fluids (D5-0.45%NS) -reduce insulin drip to 0.05 units/kg/hr. Continue until anion gap closes, NOT just until BG normalizes. This is the most common resident mistake.
Resolution Criteria UPDATED 2024
Preferred (when BHB available):
- Beta-hydroxybutyrate (BHB) < 0.6 mmol/L
- AND patient tolerating PO / clinically improved
- Venous pH ≥ 7.3
- Serum bicarbonate ≥ 18 mEq/L
- Anion gap ≤ 10 mEq/L
ADA/EASD Consensus, 2024
🔄 What changed in 2024: BHB < 0.6 mmol/L is now the preferred resolution marker. Anion gap closure was a noisy endpoint, large-volume NS gives hyperchloremic acidosis, so the gap can stay wide even after ketones clear and patients get stuck on the drip. BHB measures the actual ketoacid driving DKA. Other changes: bicarb threshold raised from ≥ 15 to ≥ 18, the anion gap removed entirely as a criterion (it is retained only where ketone testing is unavailable), and glucose < 200 downgraded to a desirable extra (you can resolve DKA while still hyperglycemic, and euglycemic DKA exists).
Transitioning to Subcutaneous Insulin
Give SQ long-acting insulin 2 hours before stopping the drip (overlap is mandatory to prevent rebound ketoacidosis) ADA/EASD Consensus, 2024. Resume home insulin regimen if known, or start TDD calculation (0.5–0.8 units/kg/day). Ensure patient is eating and K⁺ > 3.5.
When to Escalate to ICU
- pH < 7.0 or bicarb < 10
- Altered mental status / decreased GCS
- Hemodynamic instability not responding to fluids
- K⁺ < 3.0 or > 6.0 with ECG changes
- Concurrent MI, stroke, or surgical emergency
Swipe for more examples
📋 Case 1, DKA Insulin Drip Management
Patient: 28F with T1DM, glucose 520, pH 7.15, bicarb 8, AG 28, K⁺ 5.8
| Time | Action |
|---|---|
| Hour 0 | Start insulin drip 0.1 units/kg/hr fixed rate (no bolus). NS 1L/hr. Do NOT give K⁺ yet (K⁺ > 5.2). |
| Hour 2 | Glucose 380 (↓140). K⁺ 4.5 → start KCl 20 mEq/hr in IV fluids. Continue insulin drip. |
| Hour 4 | Glucose 280 (↓100/hr -on target). K⁺ 3.8 → increase KCl to 40 mEq/hr. AG closing (18). |
| Hour 6 | Glucose 240 → approaching 250 threshold. Switch fluids to D5 1/2NS + KCl to prevent hypoglycemia while continuing insulin to clear the ketones (follow BHB, not the anion gap). |
| Hour 8 | Glucose 190, pH 7.32, bicarb 16, AG 12 (closing). K⁺ 4.0. |
| Hour 10 | BHB 0.4, pH 7.38, bicarb 20, patient eating. → Overlap SC insulin (give long-acting + meal dose), wait 2 hours, THEN stop drip. |
Key: Never stop insulin drip until: (1) BHB < 0.6 mmol/L (or if BHB unavailable, AG ≤ 10), (2) pH ≥ 7.3, (3) bicarb ≥ 18, (4) patient eating, AND (5) SC insulin given ≥ 2h prior.
📋 Case 2, Euglycemic DKA (SGLT2 Inhibitor)
Patient: 52F with T2DM on empagliflozin + metformin. Presents with nausea, vomiting, abdominal pain × 2 days. Glucose 185 (not elevated!). pH 7.18, bicarb 10, AG 24, ketones 5.2.
The trap: Glucose is near-normal → team almost missed DKA. SGLT2 inhibitors cause glycosuria → glucose stays low while ketoacidosis develops.
Treatment:
- Stop empagliflozin immediately. Effects last 24–48h even after stopping.
- Start D5NS + insulin drip, need dextrose from the start since glucose is already normal. Cannot let glucose drop further.
- Aggressive K⁺ monitoring, same protocol as classic DKA.
- Clear the ketones: Same endpoints, BHB < 0.6 mmol/L with pH > 7.3 or bicarb ≥ 18. Takes longer than classic DKA because you're limited by how fast you can run insulin with dextrose.
Key lesson: Always check a VBG/BMP on any patient on SGLT2i presenting with nausea/vomiting. Normal glucose does NOT rule out DKA. Check ketones and AG.
📋 Case 3, DKA with Severe Hypokalemia
Patient: 19M with T1DM, found unresponsive. Glucose 680, pH 6.95, bicarb 4, AG 36. K⁺ = 2.8.
Critical decision: K⁺ < 3.5 → DO NOT start insulin yet. Insulin drives K⁺ intracellular → can cause fatal arrhythmia.
Treatment:
- Step 1: IV KCl 40 mEq/hr via central line (peripheral max 10 mEq/hr). Continuous telemetry. Recheck K⁺ every 1–2 hours.
- Step 2: Aggressive IVF, NS 1L/hr. Fluids alone will lower glucose ~50–75 mg/dL/hr.
- Step 3: Once K⁺ > 3.5 → START insulin drip at 0.1 units/kg/hr. Continue K⁺ replacement aggressively.
- Step 4: Consider bicarb ONLY if pH < 6.9 (give 100 mL of 8.4% NaHCO₃ in 400 mL sterile water over 2h). Controversial but ADA allows at pH < 6.9.
Key lesson: Always check K⁺ BEFORE starting insulin in DKA. K⁺ < 3.5 = replace first. This is the most dangerous moment in DKA management, insulin without adequate K⁺ kills.
💊 Medications & Doses
Medications & Dosing
| Drug | Dose / Route | Indication | Key Points |
|---|---|---|---|
| Regular Insulin | 0.1 units/kg/hr IV fixed-rate infusion, no bolus required ADA/EASD Consensus, 2024 |
Insulin infusion | Do not start if K⁺ < 3.5. Reduce to 0.05 when BG < 250 |
| Normal Saline (0.9%) | 1–1.5 L over 1 hr, then 250–500 mL/hr | Volume resuscitation. LR is an acceptable alternative (SMART, 2018 -balanced crystalloids reduce AKI/death vs NS in critically ill) | Switch to 0.45%NS after initial bolus based on corrected Na⁺ |
| KCl | 20–40 mEq/hr IV (max 40 mEq/hr via central line) 10–20 mEq/hr peripheral |
Hypokalemia in DKA | Continuous cardiac monitoring. Expect K⁺ to drop as insulin given |
| Sodium Bicarbonate | 100 mEq in 400 mL D5W over 2 hrs | pH < 6.9 only | Controversial. May worsen hypokalemia and CNS acidosis. Use sparingly |
| Phosphate | 20–30 mmol IV over 6 hrs | PO₄ < 1.0 mg/dL with symptoms | Routine replacement not recommended. Risk of hypocalcemia |
| Glargine (Lantus) | 0.25–0.3 units/kg SQ (or prior home dose) | Transition off drip | Give 2 hours before stopping drip. Do not skip |
📋 On Rounds
Common Pimp Questions
Why should you NOT start insulin if K⁺ < 3.5?
Insulin drives K⁺ intracellularly. Starting insulin when K⁺ is already low can cause life-threatening hypokalemia and fatal cardiac arrhythmia. Always replete first.
When do you stop the insulin drip?
Per ADA/EASD 2024: BHB < 0.6 mmol/L AND patient eating. If BHB unavailable, use the fallback triad: pH ≥ 7.3, bicarb ≥ 18, AG ≤ 10. NOT just when glucose normalizes. And give long-acting SQ insulin 2 hours before stopping the drip to prevent rebound ketosis.
What is euglycemic DKA and who is at risk?
DKA occurring with near-normal glucose (< 200 mg/dL). Seen with SGLT2 inhibitors (empagliflozin, dapagliflozin, canagliflozin). They enhance renal glucose excretion, masking hyperglycemia while ketoacidosis progresses. Always check ketones in SGLT2i users with nausea/vomiting.
Why is bicarbonate therapy generally avoided in DKA?
Bicarb worsens hypokalemia, may cause paradoxical CNS acidosis (buffering acid generates CO₂, and that CO₂ diffuses across the blood-brain barrier into the CSF faster than the bicarbonate itself, so CSF pH paradoxically drops), and has not been shown to improve outcomes. Reserve for pH < 6.9 only.
Clinical Examples
📋 Case 1, Classic DKA with Insulin Omission
Patient: 24 y/o F with T1DM, ran out of insulin 3 days ago, presents with nausea, vomiting, abdominal pain, and Kussmaul breathing.
Key findings: HR 118, BP 98/62, RR 28. BG 480, pH 7.12, bicarb 6, AG 28, K⁺ 5.4, BHB 6.8 mmol/L.
Management:
- NS 1L bolus over 1h, then 0.45% NS at 250 mL/hr
- K⁺ 5.4 (>3.5), start regular insulin drip at 0.1 units/kg/hr fixed rate (no bolus) ADA/EASD Consensus, 2024
- Add KCl 20 mEq/L to each liter of IVF (total body K⁺ depleted despite normal serum K⁺)
- When BG < 250, add D5 to IVF and reduce insulin to 0.05 units/kg/hr
Teaching point: Serum K⁺ is artificially elevated due to acidosis-driven transcellular shift. Total body K⁺ is always depleted in DKA. Aggressively replete as insulin drives K⁺ intracellularly.
📋 Case 2, Euglycemic DKA on SGLT2 Inhibitor
Patient: 58 y/o M with T2DM on empagliflozin and metformin, presents with 2 days of nausea, vomiting, and fatigue after a GI illness.
Key findings: BG 185, pH 7.22, bicarb 12, AG 22, BHB 5.2 mmol/L. K⁺ 4.1.
Management:
- Recognize euglycemic DKA, glucose near-normal but AG acidosis with ketones
- Hold SGLT2 inhibitor immediately
- Start insulin drip + D10 infusion (glucose already low, needs dextrose from the start)
- Volume resuscitate aggressively, SGLT2i causes osmotic diuresis
Teaching point: SGLT2 inhibitors mask hyperglycemia by enhancing renal glucose excretion. Always check ketones in SGLT2i users presenting with nausea/vomiting, even if glucose is normal.
📋 Case 3, DKA with Severe Hypokalemia
Patient: 31 y/o F with T1DM, presenting with DKA triggered by UTI. Found altered in the ED.
Key findings: BG 520, pH 7.08, bicarb 5, AG 30, K⁺ 2.9, ECG shows U waves and prolonged QTc.
Management:
- DO NOT start insulin, K⁺ < 3.5 is an absolute contraindication
- Aggressive K⁺ repletion: KCl 40 mEq/hr IV via central line with continuous telemetry
- Start insulin ONLY when K⁺ ≥ 3.5 (recheck q1h during repletion)
- Treat UTI precipitant with appropriate antibiotics
Teaching point: Insulin before K⁺ repletion in hypokalemic DKA causes fatal arrhythmias. This is the single most important safety rule in DKA management.
What to Say on Rounds
📋 Sample Presentation
"Mr. Smith is a 32-year-old with Type 1 DM presenting with a 2-day history of nausea, vomiting, and abdominal pain in the setting of missed insulin doses. He was found to have a glucose of 420, pH 7.18, bicarb of 10, and an anion gap of 24, consistent with severe DKA. He was started on NS resuscitation and a regular insulin drip at 0.1 units/kg/hr after K⁺ was confirmed to be 3.8. Over the past 8 hours, his glucose has come down to 240, his BHB has fallen from 5.2 to 1.4, and his bicarb is now 16. We are targeting a BHB below 0.6 with a pH above 7.3 before transitioning to subcutaneous insulin, rather than following the anion gap, which stays open with saline-induced hyperchloremic acidosis. His precipitant appears to be medication non-adherence, and we are involving diabetes education."
Monitoring Schedule
During Active DKA
- Glucose: every 1 hour (via POC meter)
- BMP (or at least K⁺, bicarb): every 2–4 hours
- Anion gap: calculated every 2–4 hours to confirm closure
- Beta-hydroxybutyrate: every 4 hours (preferred over urine ketones)
- Urine output: target ≥ 0.5 mL/kg/hr -place Foley if needed
- ECG: if K⁺ < 3.0 or > 6.0
Pitfalls to Watch
- Stopping insulin too early -always wait for AG closure, not just BG normalization
- Forgetting the 2-hour overlap when transitioning to SQ insulin
- Overcorrecting fluids -iatrogenic fluid overload, especially in elderly or cardiac patients
- Missing the precipitant -always ask: why did they get DKA?
- Euglycemic DKA on SGLT2i -BG may be near-normal; check ketones regardless
- Cerebral edema -rare in adults but watch for headache, declining GCS during treatment
Complications
- Hypokalemia (from insulin shifting K⁺ intracellular)
- Hypoglycemia (from excess insulin or failure to add dextrose)
- Cerebral edema (especially children, rapid fluid shifts)
- ARDS (from aggressive fluid resuscitation)
- Thrombosis (hypercoagulable state)
Before Discharge
- Patient tolerating PO fluids and meals
- On appropriate SQ insulin regimen
- BHB < 0.6, pH ≥ 7.3 or bicarb ≥ 18, K⁺ repleted, eating
- Precipitant identified and addressed
- Diabetes education arranged
- Endocrine follow-up within 1–2 weeks
⚡ Summary
One-Screen Summary
The 2024 Diagnostic Triad
All three are required: hyperglycemia (or a known diabetes diagnosis), ketosis, and metabolic acidosis. Beta-hydroxybutyrate 3.0 mmol/L or above is the preferred ketone marker, not urine ketones, which measure acetoacetate and can look falsely reassuring early and falsely persistent late. Severity is now graded on pH and bicarbonate only; anion gap and mental status were dropped.
Fluids First
Isotonic crystalloid 1 to 1.5 L in the first hour, then 250 to 500 mL/h, switching to half-normal saline if the corrected sodium is high. Balanced crystalloid is preferred over normal saline, which causes a hyperchloremic acidosis that keeps the bicarbonate low after the ketosis has cleared and makes the patient look untreated. Restoring perfusion alone lowers the glucose substantially.
Check Potassium Before Insulin, Every Time
Ensure potassium is at least 3.5 mEq/L before starting insulin. Total body potassium is depleted even when the serum level is normal or high, because acidosis and insulin deficiency drive it out of cells. Insulin given into hypokalemia causes fatal arrhythmia. Add 20 to 40 mEq per liter once the level is below 5.3 and the patient is making urine.
Insulin Infusion Without a Bolus
Regular insulin 0.1 units/kg/h. Target a glucose fall of 50 to 75 mg/dL/h. Add dextrose once the glucose reaches about 200 and continue the insulin, because the target is closing the anion gap, not normalizing the glucose. Stopping insulin at a normal glucose leaves the ketosis running.
Track the Gap, Not the Sugar
Resolution is a closed anion gap with a bicarbonate above 15 to 18 and a beta-hydroxybutyrate below 0.6, not simply a normal glucose. Urine ketones stay positive after resolution, because acetoacetate rises as beta-hydroxybutyrate is metabolized, so following them causes unnecessarily prolonged treatment.
Overlap the Transition Off the Drip
Give subcutaneous basal insulin 2 to 4 h before stopping the infusion. IV insulin has a half-life of minutes, so stopping it cleanly puts a type 1 patient straight back into ketoacidosis. The patient must also be eating and the gap closed before the drip comes down.
Hunt the Precipitant: the 5 I's
Infection (30 to 40%, the commonest, from urine, chest or skin), Insulin missed or under-dosed, Infarction (MI, stroke, mesenteric ischemia), Intoxication, Inflammation (pancreatitis). Fever is often absent, so a normal temperature does not exclude sepsis, and a troponin and ECG are worth doing in the older patient.
Two Things Not to Do, and One Not to Miss
Do not give bicarbonate except at a pH below about 6.9: it worsens intracellular acidosis, delays ketone clearance and causes hypokalemia. Do not give routine phosphate unless it is severely low or there is cardiac or respiratory compromise. Do not miss euglycemic DKA in SGLT2 inhibitor users, where the glucose can be below 200; an anion-gap acidosis with ketones in an acutely ill patient on one of these drugs is DKA until proven otherwise, treated with insulin plus dextrose. Cerebral edema is the leading cause of death in children, which is why fluid is given more cautiously in pediatrics.
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ICU / Endocrine · One Pager
Diabetic Ketoacidosis
Hyperglycemia + ketosis + acidosis. Fluids first. Check K⁺ before insulin. Clear the ketones (BHB), not just the glucose.
🧪 Diagnosis
- BG ≥ 200 mg/dL or known diabetes
- pH < 7.3 and/or Bicarb < 18
- BHB ≥ 3.0 mmol/L (or urine ketones 2+)
- Anion gap NOT a criterion (ADA/EASD 2024)
- Euglycemic DKA: BG normal on SGLT2i
⚡ Precipitants
- Infection (30–40%)
- Missed insulin (20–25%)
- New diagnosis T1DM
- MI, pancreatitis, surgery
- SGLT2 inhibitor use
🚨 Management -Step by Step
1
IV fluids: isotonic saline or balanced crystalloid 500–1000 mL/hr × 2–4h. Balanced crystalloid preferred where available (faster resolution, less hyperchloremic acidosis)
2
Check K⁺ BEFORE insulin -if < 3.5, replace first. Do NOT start insulin.
3
Insulin: fixed-rate infusion 0.1 units/kg/hr IV, a bolus is not required. HHS: 0.05 units/kg/hr. Mild DKA may use SQ rapid-acting analogue ADA/EASD 2024
4
When BG < 250: Add D5 to IVF, reduce insulin to 0.05 units/kg/hr
5
Resolved when: BHB < 0.6 mmol/L AND (pH ≥ 7.3 or bicarb ≥ 18); ideally BG < 200. Do NOT use the anion gap or urine ketones
6
SQ insulin overlap: Give basal insulin 1–2h before stopping drip, once eating
💊 Key Drugs
Regular insulin0.1 u/kg/hr
KCl20–40 mEq/hr IV
Saline / balanced crystalloid500–1000 mL/hr × 2–4h
Glargine0.25 u/kg SQ
📊 Monitoring
- BG every 1h (POC)
- BMP q2–4h
- BHB q2–4h (the marker to follow)
- Venous pH q2–4h until resolved
- UOP ≥ 0.5 mL/kg/hr
⚠️ Pitfalls
- Insulin with K⁺ < 3.5
- Stopping drip at BG normal
- Missing euglycemic DKA
- No SQ overlap
- Missing precipitant
🏥 ICU Threshold
- pH < 7.0 / bicarb < 10
- Altered mental status
- Hemodynamic instability
- K⁺ < 3.0 with ECG changes
🎓 Key Trial
- ADA/EASD 2024: BHB replaces the anion gap for diagnosis and resolution
- Resolution: BHB < 0.6; hyperchloremic acidosis from saline keeps the gap open
- Bicarb: Only if pH < 7.0 (not routine)
Rounds · ICU / Endocrine
Based on the ADA/EASD/JBDS/AACE/DTS consensus report on hyperglycemic crises, Diabetes Care 2024